Behavioural Neurology

Background and Aim. Schizophrenia is a complex psychiatric disorder with an unknown etiology. Previous studies suggest that apoptosis is potentially involved in the pathophysiology of schizophrenia, but whether apoptotic markers can help diagnosis of schizophrenia has not been reported. This study aimed to establish a potential diagnostic model based on apoptosis-related gene expression in blood samples and to construct a competing endogenous RNA (ceRNA) network that could provide mechanistic insight of schizophrenia. Methods. Gene expression profiles and apoptosis-related data were downloaded from the Gene Expression Omnibus and Molecular Signature databases, respectively. Apoptosis-related differentially expressed mRNAs (DEGs) and miRNAs (DEMs) from blood samples between the schizophrenia and healthy control individuals were screened. A diagnostic model was developed using the data from univariate and least absolute shrinkage and selection operator (LASSO) regression analyses, followed by validation using the GSE38485 dataset. Cases were divided into low-risk (LR) and high-risk (HR) groups based on the risk score of the model, and differences in immune gene sets and pathways between these two groups were compared. Finally, a ceRNA network was constructed by integrating long non-coding RNAs (lncRNAs), DEMs, and DEGs. Results. A diagnostic model containing 15 apoptosis-related genes was developed and its diagnostic efficiency was found to be robust. The HR group was correlated with higher immune scores of chemokines, cytokines, and interleukins; it was also significantly involved in pathways such as pancreatic beta cells and early estrogen response. A ceRNA network composed of 2 lncRNAs, 14 miRNAs, and 5 mRNAs was established. Conclusions. The established model is a potential tool to improve the diagnostic efficiency of patients with schizophrenia, and the nodes included in the ceRNA network might serve as biomarkers and therapeutic targets for schizophrenia.

In nicotine withdrawal (NW) conditions, molecular changes, such as increasing corticotropin-releasing factor (CRF) in the amygdala, and melanocortin signaling in the hypothalamus, can occur in the brain, leading to increased feeding behavior and body weight as somatic changes as well as high anxiety-like behavior as an affective changes. Therefore, this research aimed to investigate the effect of epigallocatechin gallate (EGCG), the largest component in green tea, on CRF, pro-opiomelanocortin (POMC), and melanocortin four receptor gene expression in the brain under NW conditions. The 24 Balb/c male mice used were randomly divided into four groups. The doses used included normal saline 1.0 mL/kg as a control group, and nicotine 3.35 mg/kg that was administered subcutaneously three times a day. After NW conditions, EGCG 50 mg/kg was administered intraperitoneally two times a day. Behavior evaluation was performed to measure somatic and affective changes, and the animal was sacrificed for molecular analysis. The results showed that NW conditions significantly increased food intake, body weight, and anxiety-like behavior compared with the normal group. Meanwhile, EGCG significantly decreased food intake, body weight, and anxiety-like behavior compared with NW conditions in mice without EGCG. The polymerase chain reaction results also showed that EGCG decreased the CRF mRNA expression in the amygdala and increased the POMC. This indicated that EGCG improved somatic and affective behavior in NW conditions by decreasing CRF mRNA expression in the amygdala and increasing POMC mRNA expression in the hypothalamus.

Vitamin B6 (VB₆) exhibits therapeutic effects towards autism spectrum disorder (ASD), but its specific mechanism is poorly understood. Rat dams were treated with VB₆ standard, VB₆ deficiency, or VB₆ supplementary diet, and the same treatment was provided to their offspring, with their body weights monitored. Three-chambered social test and open field test were employed to evaluate the effect of VB₆ on autism-like behaviors. Gamma-aminobutyric acid (GABA) generation and synaptic inhibition of neurons in the hippocampus of rat were detected via immunofluorescence staining, followed by the measurement of GABA concentration through high-performance liquid chromatography (HPLC). The role of VB₆ in the autophagy and apoptosis of cells was determined via Western blot and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). In order to conduct rescue experiments, the inhibition of mammalian target of rapamycin (mTOR) or the activation of GABA was achieved by drug administration to the offspring rats with VB₆ deficiency. As a result, no evident difference in weight was observed in the offspring with varied VB₆ treatments. VB₆ deficiency impaired social interaction; aggravated self-grooming and bowel frequency; decreased GABA concentration, VIAAT, GAD67, vGAT expressions, and LC3 II/LC3 I ratio; increased p62 level and p-mTOR/mTOR ratio; and promoted cell apoptosis. Inhibition of mTOR reversed the effect of VB₆ deficiency on cell autophagy. GABA activation or mTOR inhibition offset the role of VB₆ deficiency in autism-like behaviors and hippocampal GABA expression. Collectively, VB₆ deficiency induces autism-like behaviors in rats by regulating mTOR-mediated autophagy in the hippocampus.

Neural plasticity promotes the reorganization of language networks and is an essential recovery mechanism for poststroke aphasia (PSA). Neuroplasticity may be a pivotal bridge to elucidate the potential recovery mechanisms of acupuncture for aphasia. Therefore, understanding the neuroplasticity mechanism of acupuncture in PSA is crucial. However, the underlying therapeutic mechanism of neuroplasticity in PSA after acupuncture needs to be explored. Excitotoxicity after brain injury affects the activity of neurotransmitters and disrupts the transmission of normal neuron information. Thus, a helpful strategy of acupuncture might be to improve PSA by affecting the availability of these neurotransmitters and glutamate receptors at synapses. In addition, the regulation of neuroplasticity by acupuncture may also be related to the regulation of astrocytes. Considering the guiding significance of acupuncture for clinical treatment, it is necessary to carry out further study about the influence of acupuncture on the recovery of aphasia after stroke. This study summarizes the current research on the neural mechanism of acupuncture in treating PSA. It seeks to elucidate the potential effect of acupuncture on the recovery of PSA from the perspective of synaptic plasticity and integrity of gray and white matter.

It is well-established that light therapy can alleviate cognitive impairment, and ambient illumination (AI) can quantify the amount of exposure to light. However, the relationship between AI and cognitive impairment has been largely understudied. Objectives. We aimed to examine the cross-sectional associations between AI and impaired cognition using data from the National Health and Nutrition Examination Survey (NHANES) (2011–2013) database. Methods. The correlation between AI and cognitive impairment was analyzed using multivariate logistic regression models. Nonlinear correlations were explored using curve fitting. Results. Multivariate logistic regression yielded an OR of 0.872 (95% CI 0.699, 1.088) for the association between AI and cognitive impairment after adjusting for covariates. Smooth curve fitting showed that the correlation was nonlinear, with an inflection point at 1.22. Conclusions. These results suggested that the level of AI may be linked to cognitive impairment. We found a nonlinear relationship of AI with cognitive impairment.

The current study was planned to assess the neuropharmacological benefits of the Cucurbita maxima seed. These seeds have been conventionally used for the nutritional as well as amelioration of various diseases. However, there was a need to provide a pharmacological basis for such use. Four central nervous system-related functions, that is, anxiety, depression, memory, and motor coordination, were evaluated, and the levels of brain biogenic amines were also assessed. Anxiety was evaluated through selected experimental models, such as light and dark apparatus, elevated plus maze, head dip, and open field test. The head dip test was mainly used to assess exploratory behavior. Depression was assessed by two animal models, that is, the forced swim test and tail suspension test. Memory and learning ability were assessed by the passive avoidance test, stationary rod apparatus, and Morris’s water maze test. Motor skilled learning was assessed by stationary rod and rotarod apparatus. Reversed phase high-pressure liquid chromatography was used to determine biogenic amine levels. Results reveal that C. maxima exhibited anxiolytic and antidepressant effects with memory improvement. There was a reduction in the weight of the animal following chronic administration. Furthermore, no remarkable effects were observed on motor coordination. Norepinephrine was found elevated, which may be linked to its antidepressant effects. These biological effects of C. maxima may be due to the presence of secondary metabolites, such as cucurbitacin, beta-sitosterol, polyphenolic compounds, citrulline, kaempferol, arginine, β-carotene, quercetin, and other antioxidants. The outcomes of the present study authenticate that the chronic use of C. maxima seeds reduces the intensity of neurological problems like anxiety and depression.